Protective effect of rosiglitazone on chronic renal allograft dysfunction in rats

Deng, Jin; Xia, Yue; Zhou, Qin; Wang, Xin; Xiong, Chengliang; Shao, Xiaofei; Shao, Mengjiao; Zou, Hequn

doi:10.1016/j.trim.2019.01.002

Cited by 17 publications

(14 citation statements)

References 52 publications

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“…41 Moreover, our previous study in a chronic renal allograft dysfunction model demonstrated that PPAR-γ agonists inhibit NF-κB activation and infiltration of inflammatory cells into the interstitium. 42 In the present study, we showed that activation of PPAR-γ with RGTZ inhibits NF-κB activation, macrophage infiltration, and reduces expression of MCP-1, RANTES, TNF-α, and IL-1β induced by hyperuricemia. These data suggest that inhibition of the inflammatory response may be another mechanism by which RGTZ attenuates the renal fibrosis and the development of HN.…”

Section: Discussionsupporting

confidence: 54%

<p>Treatment with a PPAR-γ Agonist Protects Against Hyperuricemic Nephropathy in a Rat Model</p>

Wang¹,

Deng²,

Xiong³

et al. 2020

DDDT

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Hyperuricemia is an independent risk factor for renal damage and can promote the progression of chronic kidney disease (CKD). In the present study, we employ a rat model to investigate the effects of rosiglitazone (RGTZ), a peroxisome proliferator-activated receptorgamma agonist, on the development of hyperuricemic nephropathy (HN), and we elucidate the mechanisms involved. Methods: An HN rat model was established by oral administration of a mixture of adenine and potassium oxonate daily for 3 weeks. Twenty-four rats were divided into 4 groups: sham treatment, sham treatment plus RGTZ, HN, and HN treated with RGTZ. Results: Administration of RGTZ effectively preserved renal function, decreased urine microalbumin, and inhibited interstitial fibrosis and macrophage infiltration in a rat HN model. RGTZ treatment also inhibited TGF-β and NF-κB pathway activation, decreased expression of fibronectin, collagen I, α-SMA, vimentin, MCP-1, RANTES, TNF-α, and IL-1β, and increased E-cadherin expression in the kidneys of HN rats. Furthermore, RGTZ treatment preserved expression of OAT1 and OAT3 in the kidney of HN rats. Conclusion: RGTZ attenuates the progression of HN through inhibiting TGF-β signaling, suppressing epithelial-to-mesenchymal transition, reducing inflammation, and lowering serum uric acid levels by preserving expression of urate transporters.

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Section: Discussionsupporting

confidence: 54%

<p>Treatment with a PPAR-γ Agonist Protects Against Hyperuricemic Nephropathy in a Rat Model</p>

Wang¹,

Deng²,

Xiong³

et al. 2020

DDDT

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“…Hippo signaling was predicted to be decreased and Rho signaling was predicted to be increased in the SAGN tubulointerstitium, possibly predisposing to interstitial fibrosis 36 – 38 . In addition, the SAGN interstitium also showed lack of activation of pathways that could potentially protect against the development of chronic kidney damage, such as PPARα, LXR-RXR and eNOS signaling 39 , 40 . The latter were more prominently expressed in IgAN in our study as well in a study by Liu et al 41 .…”

Section: Discussionmentioning

confidence: 99%

Differentiating Staphylococcus infection-associated glomerulonephritis and primary IgA nephropathy: a mass spectrometry-based exploratory study

Satoskar

Shapiro

Jones

et al. 2020

Sci Rep

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Staphylococcus infection-associated glomerulonephritis (SAGN) and primary IgA nephropathy (IgAN) are separate disease entities requiring different treatment approaches. However, overlapping histologic features may cause a diagnostic dilemma. An exploratory proteomic study to identify potential distinguishing biomarkers was performed on formalin fixed paraffin embedded kidney biopsy tissue, using mass spectrometry (HPLC–MS/MS) (n = 27) and immunohistochemistry (IHC) (n = 64), on four main diagnostic groups—SAGN, primary IgAN, acute tubular necrosis (ATN) and normal kidney (baseline transplant biopsies). Spectral counts modeled as a negative binomial distribution were used for statistical comparisons and in silico pathway analysis. Analysis of variance techniques were used to compare groups and the ROC curve to evaluate classification algorithms. The glomerular proteomes of SAGN and IgAN showed remarkable similarities, except for significantly higher levels of monocyte/macrophage proteins in SAGN—mainly lysozyme and S100A9. This finding was confirmed by IHC. In contrast, the tubulointerstitial proteomes were markedly different in IgAN and SAGN, with a lower abundance of metabolic pathway proteins and a higher abundance of extracellular matrix proteins in SAGN. The stress protein transglutaminase-2 (TGM2) was also significantly higher in SAGN. IHC of differentially-expressed glomerular and tubulointerstitial proteins can be used to help discriminate between SAGN and IgAN in ambiguous cases.

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“…PPAR‐γ is expressed in different parts of nephron involving glomerulus, proximal tubules, and collecting ducts, which suggests its role in renal patho‐physiology (Singh, Singh, & Bhatti, 2014). PPAR‐γ agonists have been used as insulin sensitizing agents in the management of type‐2 diabetes mellitus and have been documented to attenuate AKI, which is attributed to their anti‐oxidant, anti‐apoptotic, and anti‐inflammatory activity in nondiabetic models (Cai et al, 2018; Chandra, Miriyala, & Panchatcharam, 2017; Deng et al, 2019; Singh et al, 2016). Ciglitazone, a PPAR‐γ agonist, decreased the free radical generation and angiotensin‐II as well as thromboxane‐A 2 mediated renal vasoconstriction in glycerol‐induced AKI (Yousefipour, Hercule, Truong, Oyekan, & Newaz, 2007).…”

Section: Discussionmentioning

confidence: 99%

Stevioside protects against rhabdomyolysis‐induced acute kidney injury through PPAR‐γ agonism in rats

Kaur

Singh

et al. 2020

Drug Development Research

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We explored the potential role of peroxisome proliferator activated receptor‐γ (PPAR‐γ) in stevioside‐mediated renoprotection using rhabdomyolysis‐induced acute kidney injury (AKI) model in rats. Rhabdomyolysis refers to intense skeletal muscle damage, which further causes AKI. Glycerol (50% w/v, 8 ml/kg) was injected intramuscularly in rats to induce rhabdomyolysis. After 24 hr, AKI was demonstrated by quantifying serum creatinine, urea, creatinine clearance, microproteinuria, and electrolytes in rats. Further, oxidative stress was measured by assaying thiobarbituric acid reactive substances, generation of superoxide anion, and reduced glutathione levels. Additionally, serum creatine kinase (CK) level was assayed to determine glycerol‐induced muscle damage in rats. Pathological changes in rat kidneys were studied using hematoxylin–eosin and periodic acid Schiff staining. Moreover, the expression of apoptotic markers (Bcl‐2, Bax) in rat kidneys was demonstrated by immunohistochemistry. Stevioside (10, 25, and 50 mg/kg) was administered to rats, prior to the induction of AKI. In a separate group, bisphenol A diglycidyl ether (BADGE, 30 mg/kg), a PPAR‐γ receptor antagonist was given prior to stevioside administration, which was followed by rhabdomyolysis‐induced AKI in rats. The significant alteration in biochemical and histological parameters in rats indicated AKI, which was attenuated by stevioside treatment. Pretreatment with BADGE abrogated stevioside‐mediated renoprotection, which is suggestive of the involvement of PPAR‐γ in its renoprotective effect. In conclusion, stevioside protects against rhabdomyolysis‐induced AKI, which may be attributed to modulation of PPAR‐γ expression.

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Protective effect of rosiglitazone on chronic renal allograft dysfunction in rats

Cited by 17 publications

References 52 publications

<p>Treatment with a PPAR-γ Agonist Protects Against Hyperuricemic Nephropathy in a Rat Model</p>

<p>Treatment with a PPAR-γ Agonist Protects Against Hyperuricemic Nephropathy in a Rat Model</p>

Differentiating Staphylococcus infection-associated glomerulonephritis and primary IgA nephropathy: a mass spectrometry-based exploratory study

Stevioside protects against rhabdomyolysis‐induced acute kidney injury through PPAR‐γ agonism in rats

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